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首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >Caudal midline medulla mediates behaviourally-coupled but not baroreceptor-mediated vasodepression.
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Caudal midline medulla mediates behaviourally-coupled but not baroreceptor-mediated vasodepression.

机译:尾中线延髓介导行为耦合,但不介导压力感受器介导的血管舒缩。

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摘要

Within the caudal medulla there are two regions whose activation leads to vasodepression and bradycardia, the caudal ventrolateral medulla and a discrete region of the caudal midline medulla. This study investigated, in the halothane anaesthetized rat, the contribution of these two vasodepressor regions to "homeostatic" and "behaviourally-coupled" cardiovascular regulation. In an initial set of experiments the contribution of each of these two regions to the hypotension and bradycardia evoked by acute hypovolaemia (15% haemorrhage) was investigated. It was found that inactivation of the caudal midline medulla significantly attenuated (cobalt chloride) or completely blunted (lignocaine) the hypotension and bradycardia evoked by acute hypovolaemia. In contrast, inactivation of the caudal ventrolateral medulla using cobalt chloride, although attenuating the magnitude of the hypotension and completely blocking the bradycardia, did not delay the onset of the hypotension evoked by acute hypovolaemia. The caudal ventrolateral medulla is known to be critical in homeostatic cardiovascular control through the expression of the "baroreceptor reflex" and the hypotension and bradycardia evoked by activation of cardiopulmonary afferents. In a second series of experiments we found inactivation of the caudal midline medulla played no role in baroreflex-evoked bradycardia (i.v. phenylephrine) or the hypotension and bradycardia evoked by cardiopulmonary afferent activation (i.v. 5-hydroxytryptamine).These data suggest that the caudal midline medulla and caudal ventrolateral medulla play different roles in cardiovascular control. The caudal ventrolateral medulla is involved in mediating cardiovascular changes associated with a variety of stimuli including "homeostatic" and "behaviourally-coupled" cardiovascular changes, whereas the caudal midline medulla is critical for mediating "behaviourally-coupled" changes in arterial pressure and heart rate.
机译:在尾髓内有两个区域,它们的激活导致血管抑制和心动过缓,尾腹侧外侧延髓和尾中线延髓的离散区域。这项研究在氟烷麻醉的大鼠中研究了这两个血管加压素区域对“稳态”和“行为耦合”心血管调节的作用。在最初的一组实验中,研究了这两个区域中的每一个对急性低血容量(15%出血)引起的低血压和心动过缓的影响。已发现,使尾中线延髓失活可显着减轻(氯化钴)或完全钝化(木酚卡因)急性低血容量引起的低血压和心动过缓。相反,尽管使用氯化钴使尾侧腹外侧延髓失活,尽管减弱了低血压的程度并完全阻断了心动过缓,但并未延迟急性低血容量引起的低血压的发作。通过表达“压力感受器反射”以及激活心肺传入引起的低血压和心动过缓,尾侧腹外侧延髓在稳态心血管控制中至关重要。在第二系列实验中,我们发现尾中线延髓失活在压力反射诱发的心动过缓(iv苯肾上腺素)或心肺传入激活引起的低血压和心动过缓(iv 5-hydroxytryptamine)中没有作用。延髓和尾腹腹外侧延髓在心血管控制中起着不同的作用。尾侧腹外侧延髓参与介导与各种刺激相关的心血管变化,包括“稳态”和“行为耦合”心血管变化,而尾中线延髓对于介导动脉压和心率的“行为耦合”变化至关重要。 。

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